Pituitary Gland Flashcards
Order of hormones affected in hypopituitarism
GH Gonadotropins (FSH + LH) TSH ACTH Prolactin
Hypopituitarism causes
Hypothalamic - Kallman’s, tumour, inflammation, infection (meningitis/TB), ischaemia
Pituitary stalk - trauma, mass lesion, carotid artery aneurysm
Pituitary - Tumour, irradiation, inflammation, autoimmune, infiltration (haemochromatosis, amyloid, metastases), ischaemia
Hypopituitarism tests
Test hormones secreted and downstream hormones if necessary e.g. T4 for TSH
IGF-1 for GH axis measurement
Short Synthacten test for adrenal axis
Insulin tolerance test (CI: epilepsy, heart disease, adrenal failure)
Glucagon stimulation test if ITT CI
Arginine + GH test
MRI for hypothalamic/ pituitary lesion
What is insulin tolerance test
IV insulin given to induce hypoglycaemia in morning (water only from 22:00 night before), cortisol inc and GH secretion normally triggered
Glucose must fall below 2.2mmol/L
Normally GH>20mU/L and peak cortisol >550nmol/L
Hypopituitarism treatment
Hydrocortisone for 2˚ adrenal failure
Thyroxine if hypothyroid
Hypogonadism: Testosterone (enanthate IM 250mg every 3wks) in men and oestrogen in premenopausal women
Gonadotropin therapy needed for fertility
Somatotrophin mimics human GH
Pituitary tumour histological types
Chromophobe (70%) - Many non-secretory, half produce prolactin, few produce ACTH/GH; local pressure effect in 30%
Acidophil (15%) - Secrete GH or prolactin; local pressure effect in 10%
Basolphil (15%) - Secrete ACTH; local pressure effect rare
Pituitary local pressure effects
Headache
Visual field defect
CNIII, IV, VI palsy
Diabetes insipidus
Hypothalamic disturbances to temp, sleep + appetite
Pituitary tumour tests
MRI for intra-/supra-sellar extension
Visual field tests
Screening tests: Prolactin, IGF-1, ACTH, cortisol, TFTs, LH/FSH, testosterone in men, short Synthacten test
Glucose tolerance test if acromegaly suspected
Water deprivation if DI suspected
Pituitary tumour treatment
Trans-sphenoidal surgery unless supra-sellar extension then trans-frontal, with pre-op 100mg IV/IM hydrocortisone
Radiotherapy for residual/recurrent adenomas
HRT as needed
Steroids before levothyroxine as thyroxine may cause adrenal crisis
If prolactinoma then dopamine agonist 1st line
What is pituitary apoplexy
Rapid pituitary enlargement from bleed into tumour
Can cause mass effects, CV collapse due to acute hypopituitarism
When to suspect pituitary apoplexy
All acute: GCS drop Headache Meningism Opthalmoplegia
Pituitary apoplexy treatment
Hydrocortisone 100mg IV
Fluid balance very well controlled
±cabergoline (dopamine agonist) if prolactinoma
± surgery
Find cause e.g. predisposition to thrombosis from antiphospholipid syndrome
What is a craniopharyngioma
Situated between pituitary and 3rd ventricle floor
Craniopharyngioma presentation
Over 50% in childhood with growth failure
In adults amenorrhea, dec libido, hypothalamic symptoms, tumour mass effect e.g. visual field
Craniopharyngioma tests
CT/MRI (calcification in 50% so may be seen on skull XR)
Craniopharyngioma treatment
Surgery ± post-op radiation
Prolactin physiology
Secreted by anterior pituitary
Release inhibited by dopamine produced in hypothalamus
Hyperprolactinaemia causes
Excess production (e.g. prolactinoma)
Disinhibition through pituitary stalk compression
Dopamine antagonist use (antipsychotics, MDMA, oestrogens, metoclopramide, haloperidol, methyldopa)
Pregnancy/ breastfeeding/ stress
Hypothyroidism (due to inc TRH)
Chronic renal failure (dec excretion)
Hyperprolactinaemia presentation
Menstrual disturbance in women ED/mass effects in men Hypogonadism Osteoporosis Galactorrhoea
Hyperprolactinaemia tests
Basal prolactin (non-stressful venepuncture between 9-16h) Pregnancy test TFT U+Es MRI pituitary if other causes ruled out
Hyperprolactinaemia management
Refer to endo Dopamine agonists (bromocriptine/ cabergoline) 1st line
Microprolactinoma (<10mm) management
Bromocriptine 1.25mg PO titrated up weekly by 1.25mg/d until ~2.5mg/12h
Cabergoline is alternative but safety unknown in pregnancy
Trans-sphenoidal surgery 2nd line due to reoccurence and hormone deficiency risks
Macroprolactinoma (>10mm) management
Bromocriptine if fertility needed
Surgery followed by bromocriptine ± radiation post op, if visual symptoms or pressure effects unmanageable medically
Monitor closely if medical
Hyperprolactinaemia follow up
Monitor PRL, check for headaches/visual field loss
Medication can be decreased after 2yrs with monitoring
What is acromegaly
Phenotype of increased GH, 99% due to pituitary tumour
GH stimulates bone and soft tissue growth via secretion of IGF-1
Acromegaly presentation
Acroparasthesia (acro= extremities) Amenorrhoea Inc sweating + snoring Arthralgia + backache Acanthosis nigricans Large jaw, face, nose, hands and feet Proximal weakness + arthropathy Carpal tunnel signs in 50%
Acromegaly complications
Impaired glucose tolerance (40%), DM (~15%)
Vascular - HT, LVH, arrythmias, inc IHD + stroke risk
Neoplasia - colon ca risk
Acromegaly in pregnancy
Pregnancy may be normal, signs and chemistry may remit
Acromegaly tests
Raised glucose, Ca and PO4
If basal GH >0.4mcg/L and/or IGF-1 raised then OGTT, then if OGTT >1mcg/L (glucose normally suppresses GH) then acromegaly confirmed
MRI of pituitary fossa
Look for hypopituitarism
Visual fields/acuity
ECG/echo
Old photos
OGTT in acromegaly testing
Collect samples for GH glucose every 30 mins from 0-150
False +ves from puberty, pregnancy, hepatic/renal disease, anorexia nervosa and DM
Acromegaly treatment
Trans-sphenoidal surgery 1st line
Radiotherapy if unsuitable for surgery or as adjuvant
Somatostatin analogues (octreotide/lanreotide IM) if surgery fails
GH antagonist pegvisomant if SSA not an option, suppresses IGF-1 to normal in 90% but GH levels may rise
Acromegaly treatment follow up
Yearly: GH, IGF-1 and OGTT Visual fields Vasc assessment BMI Photos
Acromegaly prognosis
May return to normal, excess mortality mostly vasc complications
16% get diabetes with SSAs, 13% after surgery
What is diabetes insipidus
Passing lots of dilute urine (>3L/d) due to impaired water reabsorption in kidney from low ADH secretion (cranial DI) or impaired response to ADH (nephrogenic DI)
Diabetes insipidus symptoms
Polyuria/dipsia
Dehydration
HyperNa symptoms
Cranial DI causes
50% idiopathic
Congenital - DIDMOAD, ADH defects
Tumour - craniopharyngioma, metastases, pituitary
Trauma - temporary if distal to pituitary stalk
Hypophysitis/ectomy
Infiltration - sarcoidosis, histiocytosis
Haemorrhage
Meningoencephalitis
What is DIDMOAD
DI, DM, Optic atrophy, deafness
Rare autosomal recessive disorder
Also known as Wolfram’s syndrome
Nephrogenic DI causes
Inherited Metabolic - low K, high Ca Drugs - Lithium, demeclocycline Chronic renal disease Post-obstructive uropathy
Diabetes insipidus tests
Glucose (exclude DM)
U+E
Serum (285-295mOsmol/kg normally) + urine (2x serum) osmolalities
Diagnose with water deprivation tests, primary polydipsia is a differential with hypoNa
Cranial DI treatment
MRI head, test anterior pituitary function Give desmopressin (ADH analogue)
Nephrogenic DI treatment
Treat cause
Bendroflumethiazide 5mg/24h PO if persists
NSAIDs lower urine volume and plasma Na by inhibiting prostaglandin synthase (prostaglandins locally inhibit ADH action)
Diabetes insipidus emergency management
Urgent plasma U+Es and serum + urine osmolalities
IVI to keep up with urine output, use 0.9% saline initially
Lower Na slowly (lower <12mmol/L per day), any faster may cause cerebral oedema + brain injury
Desmopressin 2mcg IM (lasts 12-24h) may be used as therapeutic trial
8hr water deprivation test when to do it
When established that urine output >3L/d
8hr water deprivation test preparation
Free fluids until 7.30, light breakfast at 6.30 if starting at 8.00
No tea, coffee or smoking
8hr water deprivation test stage 1
Fluid deprivation start at 8.00
Empty bladder then no drinks, just dry food
Weigh hourly, if >3% weight lost or serum osmolality rises>300mOsmol/kg go to stage 2, if less continue stage 1
Collect urine every 2h, measure osmolality and volume
Venous osmolality sample every 4h
Stop test after 8h if urine osmolality >600 (normal)
8hr water deprivation test stage 2
Distinguish between nephrogenic + cranial
Give desmopressin 2mcg IM, can drink water now
Measure urine osmolality hourly for 4h
8hr water deprivation test urine osmolality result interpretations
If normal, urine:plasma osmolality ratio >2
If 1˚ polydipsia, urine concentrates but less than normal e.g. >400-600mOsmol/kg
If cranial DI, urine osmolality increase >600 after desmopressin, if ambiguous then extended water deprivation test (from 18.00 night before, no water)
If nephrogenic DI, no inc in urine osmolality after desmopressin
What is SIADH
Syndrome of inappropriate ADH secretion, even when low plasma osmolality/ large plasma volume
SIADH diagnosis
Concentrated urine (Na>20mmol/L and Na osmolality >100mOsmol/kg) with hyponatraemia and low plasma osmolality
